Case No. 1
A 37-year-old man was brought to the emergency department by fire rescue with the complaint of “cocaine [‘crack’] reaction.” According to the paramedics responding to the call, the patient was combative and hallucinating on the scene. Insertion of an intravenous line was attempted en route, but the line could not be established because of the patient’s uncooperative behavior.
On arrival at the emergency department, the patient became momentarily unresponsive and was notably diaphoretic. Initial vital signs were as follows: temperature, 38.8°C (101.9°F); radial pulse, 139 and regular; respiratory rate, 40; and blood pressure, 143/87.
An intravenous line of normal saline solution was established. Within minutes, the patient began to respond to his name.
Blood specimens were obtained, including one to determine a room-air arterial blood gas (ABG) level, which showed the following results:
Tabled
1
| ABG: | |
|---|---|
| pH: 6.85 | HCO 3: 5 |
| PCO 2: 29% | Base excess: –29 |
| PO 2: 97% | O 2 saturation: 90% |
Tabled
1
| Serum chemistries: | |
|---|---|
| Glucose: | 304 mg/dL |
| Sodium (Na+): | 140 mmol/L |
| Potassium (K+): | 4.8 mmol/L |
| Chloride (Cl): | 99 mmol/L |
Immediately after receiving the ABG results, 2 amps of sodium bicarbonate were administered by intravenous push and 2 additional amps were added to the infusing normal saline solution to correct the patient’s profound metabolic acidosis.
As the patient’s level of consciousness improved, he continued to complain of a “crampy” feeling in his lower abdomen. He then related that the lower abdominal pain began about 10 minutes after he smoked 4 rocks of crack cocaine and that he had also vomited. The abdominal assessment was unremarkable except for hypoactive bowel sounds and a notation of the patient’s obesity. Radiographic examinations of the chest and abdomen were likewise unremarkable.
Review of the patient’s medical history uncovered several previous drug-related visits, including a past ICU admission only 1 year ago for crack cocaine abuse, acute kidney failure, and rhabdomyolysis.
Additional abnormal results of blood tests were found, including the following:
Tabled
1
| Creatine phosphokinase: | 643 U/I |
| Leukocytes (white blood cells [WBCs]): | 37,900/mL |
| Platelets: | 449,000/mm3 |
| Blood urea nitrogen: | 21 mg/dL |
| Serum creatinine: | 1.7 mg/dL |
| Serum lactic acid: | 3.3 mEq/L |
A repeat room-air ABG specimen drawn 4 hours later indicated that the metabolic acidosis was being corrected:
Tabled
1
| pH: 7.35 | HCO 3: 24 |
| PCO 2:43% | Base excess: –2 |
| PO 2: 76% | O 2 saturation: 95% |
Surprisingly, the results of the first urine toxicology screen, for which a specimen was obtained approximately 30 minutes after the patient’s arrival, were negative for cocaine metabolites, cannabinoids, opiates, benzodiazepines, and amphetamines. Some persons believe that a “false-negative” urine drug screen can be attributed to the time of collection versus the time delay between metabolism of the drug and its actual excretion; however, this phenomenon remains unclear. A repeat urine specimen sent for a toxicology screen 12 hours later was positive for cocaine metabolites.
Now fully oriented, the patient continued to complain of lower abdominal pain. The surgical team was summoned and determined that the patient was not a surgical candidate at this time. He was admitted to a medical floor under the working diagnoses of abdominal pain, rule out ischemic bowel, and rhabdomyolysis.
The patient had a full recovery and was discharged the following day.
Case No. 2
A 51-year-old homeless man came to the emergency department and reported that he had dark red blood in stools 6 hours before arrival and similar episodes during the past 3 days. The triage nurse recorded the patient as being “very drowsy” and “falling asleep as he talks.” The initial assessment of the abdomen revealed mid-abdominal pain and a soft and nontender abdomen. The patient denied having a medical history of gastrointestinal bleeding, but he admitted to recently using crack cocaine and alcohol and having been an intravenous drug abuser for 37 years.
The patient’s initial vital signs at triage were as follows: oral temperature, 36.1°C (96.9°F); pulse, 42 and regular; respiratory rate, 18; and initial blood pressure, 64/44. The triage nurse re-assessed the blood pressure as 72/52 a few moments after the initial reading.
A subclavian line was established (establishing a peripheral line was not possible because the patient’s veins were sclerotic as a result of his extensive history of intravenous drug abuse) and normal saline solution was rapidly infused to correct the patient’s hypotension. After 1 L of normal saline solution was infused, the patient’s blood pressure reached 100/66 and later stabilized at 119/83.
The patient’s abdomen was assessed as nondistended, with bowel sounds present, and diffusely tender to palpation. A right inguinal hernia was noted, but no guarding, no rebound tenderness, and no ecchymoses were seen on physical examination. Results of a rectal examination were positive for occult blood.
Pertinent hematology results were as follows:
Tabled
1
| Leukocytes (WBCs): | 5900/mL |
| Erythrocytes (red blood cells): | 3.79 million/mL |
| Hemoglobin: | 12.4 g/dL |
| Hematocrit: | 37% |
| Platelets: | 145,000/mm3 |
| Prothrombin time/partial thromboplastin time: | 13.0/28 |
Serum chemistries (including amylase and lipase) were normal except for the following:
Tabled
1
| Serum calcium (Ca++): | 8.3 mg/dL |
| Serum albumin: | 2.9 g/dL |
| Direct serum bilirubin: | 0.5 mg/dL |
| Serum glutamate oxalo-acetate transaminase: | 66 units/L |
Results of the urine toxicology screen were positive for cocaine, opiates, and benzodiazepines.
An acute abdominal x-ray series (a chest film and flat and upright abdominal films) displayed a nonspecific bowel gas pattern with no free air noted under the diaphragm.
Following stabilization in the emergency department, the patient was admitted to a medical team for observation of a gastrointestinal bleed. The patient’s bleeding resolved during the otherwise uneventful hospital stay, and he was subsequently discharged with scheduled medical follow-up.
Case No. 3
A 37-year-old man came to the emergency department and reported having generalized abdominal pain with nausea and vomiting after using crack cocaine.
The patient’s initial vital signs were as follows: oral temperature, 37.0°C (98.6°F); pulse, 80 and regular; respiratory rate, 20; and blood pressure, 114/80.
Additional assessment findings noted that the patient was having difficulty ambulating because of abdominal pain.
The abdominal assessment revealed no bowel movement for the past 2 days, periumbilical pain with bowel sounds present in all 4 quadrants, no rebound tenderness, negative Rovsing’s sign, negative psoas sign, and negative McBurney’s sign.
The patient denied taking daily medications, had no allergies, denied alcohol use, and had no significant medical history other than crack cocaine abuse.
An intravenous infusion of lactated Ringer’s solution was established, and blood specimens were obtained and sent to the laboratory for analysis. The abnormal laboratory results were as follows:
Tabled
1
| Leukocytes (WBCs): | 17,800/mL |
| Urine bile: | Positive |
| Serum amylase: | 242 mmol/L |
| Serum lipase: | 335 units/L |
An acute abdominal radiographic examination was ordered, and the upright kidneys, ureter, bladder (abdominal film) clearly defined free air under the diaphragm consistent with an intra-abdominal perforation. The surgical team was summoned, and the patient was prepared for an emergent exploratory laparotomy.
The surgeon’s postoperative note read: “Perforated pyloric ulcer secondary to ‘crack’ use…Graham patch [performed] in OR.”
These selected case reviews represent 3 actual patients who abused crack cocaine and came to the emergency department with “crack bellies” (abdominal pain associated with crack cocaine use), along with the sequelae of their visits.
Crack cocaine
“Crack,” a less expensive form of cocaine, entered the United States’ illicit drug scene in the 1980s, bringing with it yet another challenge for drug enforcement agencies and emergency departments alike. Crack is the slang or street name given to cocaine that has been processed from cocaine hydrochloride to a free base for smoking (heating the compound, which is mixed with either ammonia or sodium bicarbonate [baking soda] and water).
1
Cocaine hydrochloride is the white crystalline powder form derived from the coca leaves; it is either snorted or dissolved in water and injected directly into the bloodstream. The term ‘crack’ refers to the crackling sounds heard when the mixture is smoked (heated), presumably from the sodium bicarbonate.2
Illegally sold in small packets containing the pellet-size “rocks” of cocaine-base for an average street value of $5 to $10 per rock, this highly addictive and often potent compound is usually smoked in a pipe or in a marijuana cigarette to render the 5- to 10-minute euphoric state
3
or “high” its users seek. One study revealed “a greater abuse liability, a greater propensity for dependence, and more severe consequences when cocaine is smoked (cocaine-base) or injected intravenously (cocaine hydrochloride) compared with intranasal use (cocaine hydrochloride).”4
The low cost of the drug allows it to be more prevalent in lower socioeconomic classes, and the distribution is likewise more widespread in the larger inner cities.
3
Abusers often gather in abandoned houses or buildings to purchase, use, and share the product (thus the term “crack houses”).In 1994, the National Household Survey on Drug Abuse estimated that “1.4 million Americans were current cocaine users” and of that rate “an estimated one-half million were current ‘crack’ cocaine users.”
5
According to a 1996 survey conducted by the National Institute on Drug Abuse, “22 million Americans age 12 and older had tried cocaine at least once in their lifetimes; about 4.0 million had used cocaine during the past year; and about 1.7 million had used cocaine in the past month.”1
While the National Institute on Drug Abuse study of 1996 pointed out that the statistics represented significant decreases in cocaine use from its peak of nearly 5.7 million users in the United States in 1985, the data collected by the Drug Abuse Warning Network (DAWN) in 1996 shows alarming increases in cocaine-related ED cases. The DAWN survey revealed that after a significant decline from 101,578 cases in 1988 to 80,355 in 1990, the number of incidents began an increasing trend in 1991 and had reached an estimated 142,494 in 1995.
1
The DAWN study data were also alarming in that the number of ED cases was highest for persons aged 35 years or older; the number of cases involving men (94,502) was twice that involving women (46,544); and blacks accounted for 77,201 of the cases, whites for 41,700 cases, and Hispanics for 11,581 cases.
1
Crack cocaine remains today’s dominant illicit drug problem in the United States.5
Because of its often rushed and uncontrolled production, the purity of the drug is unpredictable, as are its effects. A myriad of cases have been documented in which cocaine has been attributed to acute myocardial infarctions among its users.
6
, 7
Another documented complication is rhabdomyolysis8
, 9
(a condition precipitated by muscle mass breakdown to meet the body’s demand for energy).8
Biochemical abnormalities found in rhabdomyolysis include hyperkalemia, hyperphosphatemia, hyperuricemia, increased creatinine phosphokinase activity, elevated serum creatinine, and myoglobinuria.
8
When death occurs [from rhabdomyolysis], it tends to be secondary to complications of hyperkalemia, excessive fluid administration, disseminated intravascular coagulation, or respiratory distress syndrome.8
However, lesser known and relatively recently identified complications seen among some crack cocaine abusers are ischemic bowel syndromes
10
, 11
and gastropyloric perforations,12
presumably because of the drug’s potent vasoconstrictive properties, although the exact mechanism(s) is/are not clear.This situation presents an additional challenge to the ED nurse when a crack cocaine abuser has acute abdominal pain (or a “crack belly” in ED lingo). In addition to the common physical effects of cocaine (which includes constricted peripheral blood vessels, dilated pupils, and increased temperature, heart rate, and blood pressure), the patient can be hyperstimulated or “over-reactive” to stimuli in the acute euphoric state.
1
The bizarre and sometimes aggressive paranoid behavior1
exhibited by patients who abuse crack makes it difficult to aggressively investigate the crack cocaine abuser’s complaint of abdominal pain, but a thorough assessment and frequent re-assessments of the abdomen are critical.A question the emergency nurse should ask while caring for any patient complaining of abdominal pain is: “How consistent is the patient’s complaint of pain to the actual physical assessment?” The answer to that question is certainly not clear when caring for an active crack cocaine abuser and may not be revealed even in the best performed physical examination.
Conclusions
When caring for a patient who has used crack cocaine, the professional must bear in mind that the patient has an altered mental status and perceptions. When it is noted that these patients are under the influence of illicit drugs and may appear to be overreacting to external stimuli, the professional must address each complaint through proper and repeated assessments to substantiate and ascertain the severity of the complaint(s). For some crack cocaine abusers, the complaint of abdominal pain can be a medical or surgical emergency.
Acknowledgements
Acknowledgment I extend a special thanks to Dr. Michael Stary, MD, for his assistance in the literature search and retrieval for this article.
References
- Cocaine abuse. NIDA Capsules Series C-82-02.: National Institutes of Health, Washington1997
- Crack and cocaine. NIDA InfoFax 011.: National Institutes of Health, Washington1998
- NIDA InfoFax 041.: National Institutes of Health, Washington1998
- Crack cocaine and cocaine hydrochloride, are the differences myth or reality?.JAMA. 1996; 3: 1580-1588
- Facts about cocaine abuse and treatment. NIDA Notes.: National Institutes of Health, Washington1995
- Acute myocardial infarction and chest pain syndromes after cocaine use.Am J Cardiol. 1990; 66: 1434-1437
- Acute myocardial infarction shortly after cocaine inhalation.Am J Cardiol. 1987; 59: 161
- Case report: cocaine-associated rhabdomyolysis.Am J Med Sci. 1989; 297: 334-336
- Acute rhabdomyolysis associated with cocaine intoxication.N Engl J Med. 1988; 319: 673-677
- Ischemic colitis in a crack abuser.Dig Dis Sci. 1991; 36: 238-240
- Intestinal ischemia caused by cocaine ingestion, report of two cases.Surgery. 1985; 97: 374-376
- Crackrelated perforated gastropyloric ulcer.J Clin Gastroenterol. 1991; 13: 17-19
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☆For reprints, write: Mitchell G. Mason, RN, BSEd, 316 SW 194th Ave, Pembroke Pines, FL 33029.
☆☆J Emerg Nurs 1999;25:373-6.
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